Fascicular blocks

[!TIP] Mnemonics
Left fascicular block will cause axis deviation 'away' from the blocked fascicle
Posterior block will cause q wave in inferior leads ("postero-inferior")
Anterior block will cause q waves in lateral leads (?except lead I) - ("Anterolateral")

Bifascicular block
= LAFB with RBBB

"Bifascicular block is the combination of RBBB with either LAFB or LPFB" Source

Trifascicular blocks

• A "trifascicular block" is the combination of a right bundle branch block, left anterior or posterior fascicular block and a first-degree AV block (prolonged PR interval). Source

• The term “trifascicular block” is a misnomer, since the AV node itself is not a fascicle. A trifascicular block is a precursor to complete heart block.

• A true trifascicular block has a complete heart block. Source

• Class III antiarrhythmic - prolongs the action potential by blocking the rapid component of the rectifier potassium current.
• Used for rhythm control in AF,
• management of recurrent paroxysms of atrial flutter
• ventricular tachycardias.

[!TIP] Mnemonic: Light, liver, lungs, levothyroxine
Light - cataracts, photosensitivity
Liver - steatohepatitis
Lungs - fibrosis
Levothyroxine - hypothyroidism or hyperthyroidism (levothyroxine is just a mnemonic because it has L)

From pass medicine:

• Anti Hu - painful paraneoplastic neuropathy. Associated with small cell lung cancer. (Hu - Hurt -> painful neuropathy)
• Anti Ri - dancing eyes - Opsoclonus myoclonus syndrome (aka dancing eye dancing feet syndrome) (breast and ovarian cancer) (NSFW mnemonics ;) )
• Anti GAD - Seen in stiff person syndrome and Type 1 DM. (Good "gad" I feel stiff)
• Anti Yo - paraneoplastic cerebellar degeneration (seen in gynaecological cancers like ovarian and breast) (Yoyoing required coordination -> which is lost in cerebellar degenration)

Mnemonics:

Anti-Ri (Rieally blurry vision)
Anti GAD GAAAAD he's stiff (stiff man syndrome)
Anti-Hu who kicked my chair (pain) and then fell over (ataxia)
Anti yo- Yo lady give me back my danish (cerebellar syndrome, lady for breast + ovarian)

Erythrasma

• Superficial infection caused by corynebacterium minutissimum.
• Red fluorescence under wood's light.
• Treated with topical antibacterial, miconazole and if severe, oral erythromycin.

[!INFO] My classification

• In short, the sick euthyroid syndrome is a biochemical pattern of decreased circulating T3 levels, without a strong compensatory TSH response. The raised levels of rT3 result in a disproportionate degree of thyroid dysfunction, as rT3 is an inactive form, and therefore a competitive antagonist of "real" T3. - Source

• Also known as NTIS (non thyroidal illness syndrome)
• Hormone profiles are shown below.
  
  
  Source
  Biochemical profile:
• T3 : Low (peripheral conversion of T4 to T3 is reduced, therefore T4 may be increased)
• TSH : Not elevated (i.e low or normal)
• rT3 : elevated (inactive form of T3; Is a T3 antagonist)
  Source

Wernicke encephalopathy

• Mnemonic : Altered mental state + eye signs + ataxia
  • Horizontal nystagmus is typical.
  • Vertical nystagmus can occur.

[!TIP] Kor - chronic, confabulations

• Ergotamine - 5HT1 partial agonist.
• Telcagepant - newer drug.
  • Cyproheptadine - 5HT2 receptor antagonist; also has antihistamine activity.
    • Sedation and weight gain.
• Sudden worsening of muscle weakness of a patient with MG leading to respiratory failure. Most commonly begins with worsening generalized weakness, and less commonly with worsening bulbar weakness. Some can present with respiratory failure. - UpToDate.
• High morbidity with 5% mortality.
• May require prolonged ventilation.
• Needs intubation and immunotherapy with IVIG or plasmapheresis.
• Precipitated by infection (most common precipitant), surgery (eg thymectomy), medication weaning, #pregnancy or drugs listed below.
• D penicillamine
  • Fluoroquinolones

[!TIP] mnemonic: DNAAB

• Upto about 4 hours, it looks like nothing happened.
• Then the infarct slowly mottles and darkens upto about 24 hours.
• From then on, coagulative necroris changes are seen.
• Laying down of granulation tissue begins around 7 days and intensifies upto 14 days.
• Scar formation is complete by 8 weeks, the scar has formed.

• Commonest in left ventricular free wall: (rupture is commonest in anterior and lateral STEMI). It can be rapidly fatal due to haemopericardium -> tamponade.
• Papillary rupture -> Severe MR. (usually occurs 2 to 7 days post-ischemic event)
  • Source
  • This causes a "Sea-gull" murmur.
• Most commonly within 3-7 days after infarction when phagocytosis is maximal and coagulatively necrosed tissues are being removed and replaced by soft granulation tissue.
  • Use of NSAIDS

Alcohol is a common cause.
CKD, Cystic fibrosis, haemochromatosis, Obstruction, trauma, recurrent acute pancreatitis, hypercalcemia, autoimmune are all causes. Source
Also pancreatic structural abnormalities like pancreas divisum and annular pancreas.
Diagnosis:

• Low levels of faecal elastase (aka pancreatic elastase 1) suggest pancreatic insufficiency.
• X-ray and CT will show pancreatic calcification.

There is loss of endocrine and exocrine function but significant failure occurs only after many years.

• Exocrine failure becomes clinically apparent only when 90% of the pancreas is destroyed.
• Therefore, symptoms of insufficiency occur several years after the onset of chronic pain.
• Ethanol does this by increasing intracellular calcium which causes trypsin activation but alcohol must be only one factor of many which act together.
• CFTR gene (Cyctic fibrosis transmembrane conductance regulator) function is required for production of high volume bicarbonate rich pancreatic juice which flushes out trypsin. Therefore, Cystic fibrosis is associated with chronic pancreatitis.
  • In cystic fibrosis patients, pancreatic exocrine insuffiency will develop in utero or the perinatal period.
  • They will develop malabsorption and failure to thrive.
• Autoimmune pancreatitis Type I (the commonest type) is seen in men. IgG4 positive with dense lymphoplasmacytic infiltrate.
  • Autoimmune pancreatitis responds well to steroids and lack of response should arouse suspicion of another diagnosis.
  • Azathioprine is used for relapses.
• Formic acid is the toxic metabolite. (as little at 30ml of methanol can be significantly toxic needing dialysis)
• Symptoms are delayed with co-ingestion of ethanol because there is competitive inhibitions.
• There is a latent period followed by symptoms similar to ethanol intoxication with ataxia, disinhibition. (no motor weakness) #2015OCT-BOF/Q3
• Nausea, vomiting, and abdominal pain subsequently ensue,
• followed by central nervous system (CNS) depression and hyperventilation as metabolic acidosis occurs. Ocular symptoms associated with retinal toxicity are often evident in the form of blurry vision, decreased visual acuity, photophobia, and “halo vision.”
• These symptoms are associated with physical exam findings that may include papilloedema, optic disc hyperemia, and pupillary defects on fundoscopic evaluation.
  • 

• Cyanosis is common in methaemoglobinaemia.
• Cyanosis does not improve with oxygen therapy.
• The skin takes on a "chocolate cyanosis" appearance.
• Lactic acidosis can occur due to tissue hypoxia.

Causes of methaemoglobinemia

Hereditary:

• Cytochrome b5 reductase deficiency - majority
• cytochrome b5 deficiency
  Acquired:
• Dapsone : common cause- even topical treatment - (Treatment of leprosy, also used for [[2021 General Medicine July#Deramatologic manifestations of internal malignancy|Sweet syndrome]], acne)
• Recreational amyl nitrates
• Rasburicase - recombinant urate oxidase used to treat hyperurucaemia in maglinancy and tumor lysis syndrome.
• Anyline dyes used for wood finishing and textiles.
• Causes methhaemoglobinaemia with cyanosis and SpO2 around 85%.Source
• If methylene blue and exchange transfusion is not available, venesections with blood transusion can work. (Case report: Source)
• Study: Source
  
  Source
• Methylene blue.
• Example of effectiveness of methylene blue: Source
• Carey coombs - occurs during ACUTE rheumatic carditis due to mitral valve thickening.
  • Resolves when acute mitral valve carditis resolves.

[!INFO] Gallavardin phenomenon
A mid-systolic ejection murmur, heard best over the right second intercostal space, with radiation into the right neck. However, high-frequency components may radiate to the apex in calcified aortic valves, and this phenomenon is called the Gallavardin phenomenon. Source

1 unit = half a pint of beer

• Mainly auditory: Source

• Hallucinations are usually visual in Delerium tremens.
• hypophophatemia - results from malnutrition.
  Supportive - benzodiazepines to prevent progression of withdrawal symptoms. (benzodiazepines potentiate GABA binding)

Cryoglobulinaemia

#2015OCT-BOF/Q10

suspected in patients presenting with arthralgia, purpura, skin ulcers, glomerulonephritis, and peripheral neuropathy.

1. Beta blockers - see [[#Beta blocker pharmacology]] below
   1. First line anti anginal medications; Initial step in angina management is "beta blocker montherapy." Beta blockers are the ⭐only antianginals proven to reduce reinfarction and reduce mortablity.
   2. Mechanism: reduce heart rate and contractility -> reduced oxygen demand -> therefore delay the onset of angina during exercise. Also reduced LV wall stress by their antihypertensive action.
   3. Contraindicated in prinz-metal angina; unopposed alpha action may exacerbate coronary vasospasm.
2. CCBs
   1. rate liming Non-dihydropyridines are preferred when used as monotherapy.
   5. Mechanism: Coronary and peripheral vasodilation and reduced contractility.
   7. Most probably no mortality benefit Source

• Ivabradine is a selective If channel blocker and acts by reducing firing rate of pacemaker cells in the sinoatrial node, without affecting the duration of action potential. The reduction of heart rate causes a reduction of left ventricular end diastolic pressure and increases the time useful to coronary flow by a prolongation of the diastole. A body of evidence found that two drugs are useful in ischemic patients whether at rest or during exercise. In addition, they can be used in monotherapy or in association with other conventional anti-ischemic drugs

• Ivabradine cannot be given if heart rate is < 70.
• They can have visual disturbances and ⭐diplopia due to abducens nerve palsy.
• Opening pressure > 250 mmH20 confirms elevated ICP. CSF composition will be normal.
• The major morbidity associated with idiopathic intracranial hypertension (IIH) is vision loss.

The visual field loss is typically peripheral with nerve fiber bundle type defects predominating. Central defects occur in more advanced disease.
Known causes of IIH:
1. tetracyclines including doxycyline and minocycline.
2. Hypervitaminosis A (excessive dietary intake / retinoic acid, isotretinoin)
1. Avoid eating polar bear liver. ;) Source
3. COCP
4. Lithium
- chronic infection: Hep C, especially when Hep C leads to [[2022 General Medicine Paper-May#Cryoglobulinaemia|Cryoglobulinaemia]] (C for Cryo), Tuberculosis, Subacute Infective endocarditis

[[2022 General Medicine Paper-May#Cryoglobulinaemia]]

Preference of prescription of drugs in heart failure (HFrEF)

[!TIP] Mnemonic: SSL

• Spironolactone
• SGLT-2 inhibitor
• Loop diuretics

Source

[!INFO] Respiratory alkalosis
Respiratory alkalosis followed by metabolic acidosis is characteristic of salicylate poisoning.

Symptoms include

• Hyperventilation, sweating, tinnitus (stimulation of cochlear NDMA receptors), vomiting

• ECG: widened QRS, AV block, ventricular arrhythmias

  • Respiratory alkalosis occurs due to direct respiratory center stimulation by salicylate.
  • There is compensatory bicarbonate-uria. (i.e loss of bicarbonate in the urine) accompanied by urinary potassium loss --> hypokalemia

• hypokalemia

• This is followed by metabolic acidosis – lactate. There is also ketone body formation.

• Increased cellular metabolism due to uncoupling of cellular respiration causes hypoglycaemia. (neuroglycopenic symptoms can occur even when CBS is in the normal range).

• Source

• In terms of management however, whereas aspirin can be cleared from overdose victims by haemofiltration, quinine cannot be extracted easily by extracorporeal methods. Central nervous symptoms such as tinnitus, deafness and visual defects which may occur with aspirin are usually transient whereas quinine leaves permanent neural damage, if the patient survives.

• Quinine toxicity is managed by urgent alkalinization with bicar and intubation + hyperventilation.

can cause [[2022 General Medicine Paper-May#Cryoglobulinaemia|Cryoglobulinaemia]].

Colorectal cancer syndromes

• Inheritance of FAP and Lynch Synromes : #autosomalDominant
• "Polyposis" refers to the development of a large number of polyps in the GI tract. Source

Classification base on presence of pre-existing polyposis: (genes in Brackets)

• [[passMedicine Summaries#Peutz-Jeghers syndrome]]
• [[2020-NOV-BasicSciences#Lynch syndrome]]

Alkaptonuria

Source

• #autosomal-Recessive defect of phenylalanine and tyrosine metabolism.
• Also called black bone disease
• Tetrad of diagnostic features of alkaptonuria (AKU) (dark urine (A), ear (B) and eye (C) pigment and (D) joint ochronosis). The diagnosis of AKU relies on recognising the black urine present from birth, blue/black ear pigment, black scleral pigment and clinical arthritis. These features usually alert a physician into considering AKU as the diagnosis.
• Urine turns black when exposed to air.
• There is a deficiency of the enzyme HGD (Homogentisic dioxygenase) which leads to accumulation of toxic homogentisic acid. (which can be detected in the urine) (hence the black color on exposure to air)
• Usually a benign disease
• Treatment : Vitamin C Supplementation and dietary restriction of phenylalanine and tyrosine.
  • Protein controlled diet is recommended. Source

Waterhouse-Friederichsen syndrome

Bilateral adrenal haemorrhage most commonly due to meningococcal septicaemia.
Usually fatal within 24 to 48 hours.
Majority occurs in children.
Source